
@article{yu_reactomepa_2016,
	title = {{ReactomePA}: an R/Bioconductor package for reactome pathway analysis and visualization},
	volume = {12},
	issn = {1742-2051},
	url = {http://pubs.rsc.org.eproxy2.lib.hku.hk/en/content/articlelanding/2016/mb/c5mb00663e},
	doi = {10.1039/C5MB00663E},
	shorttitle = {{ReactomePA}},
	abstract = {Reactome is a manually curated pathway annotation database for unveiling high-order biological pathways from high-throughput data. {ReactomePA} is an R/Bioconductor package providing enrichment analyses, including hypergeometric test and gene set enrichment analyses. A functional analysis can be applied to the genomic coordination obtained from a sequencing experiment to analyze the functional significance of genomic loci including cis-regulatory elements and non-coding regions. Comparison among different experiments is also supported. Moreover, {ReactomePA} provides several visualization functions to produce highly customizable, publication-quality figures. The source code and documents of {ReactomePA} are freely available through Bioconductor (http://www.bioconductor.org/packages/{ReactomePA}).},
	pages = {477--479},
	number = {2},
	journaltitle = {Molecular {BioSystems}},
	shortjournal = {Mol. {BioSyst}.},
	author = {Yu, Guangchuang and He, Qing-Yu},
	urldate = {2016-02-17},
	date = {2016-01-26},
	langid = {english}
}

@article{yu_chipseeker_2015,
         title  = "ChIPseeker: an R/Bioconductor package for ChIP peak annotation, comparison and visualization",
         author = {Yu, Guangchuang and Wang, Li-Gen and He, Qing-Yu},
         journal = "Bioinformatics",
         year    = "2015",
         volume  = "31",
         number  = "14",
         pages   = "2382-2383",
         PMID    = "25765347",
	 url     = {http://bioinformatics.oxfordjournals.org/content/31/14/2382.abstract},
         doi     = "10.1093/bioinformatics/btv145",
}

@article{yu_dose_2015,
	title = {{DOSE}: an R/Bioconductor package for disease ontology semantic and enrichment analysis},
	volume = {31},
	issn = {1367-4803, 1460-2059},
	url = {http://bioinformatics.oxfordjournals.org/content/31/4/608},
	doi = {10.1093/bioinformatics/btu684},
	shorttitle = {{DOSE}},
	abstract = {Summary: Disease ontology ({DO}) annotates human genes in the context of disease. {DO} is important annotation in translating molecular findings from high-throughput data to clinical relevance. {DOSE} is an R package providing semantic similarity computations among {DO} terms and genes which allows biologists to explore the similarities of diseases and of gene functions in disease perspective. Enrichment analyses including hypergeometric model and gene set enrichment analysis are also implemented to support discovering disease associations of high-throughput biological data. This allows biologists to verify disease relevance in a biological experiment and identify unexpected disease associations. Comparison among gene clusters is also supported.
Availability and implementation: {DOSE} is released under Artistic-2.0 License. The source code and documents are freely available through Bioconductor (http://www.bioconductor.org/packages/release/bioc/html/{DOSE}.html).
Supplementary information: Supplementary data are available at Bioinformatics online.
Contact: gcyu@connect.hku.hk or tqyhe@jnu.edu.cn},
	pages = {608--609},
	number = {4},
	journaltitle = {Bioinformatics},
	shortjournal = {Bioinformatics},
	author = {Yu, Guangchuang and Wang, Li-Gen and Yan, Guang-Rong and He, Qing-Yu},
	urldate = {2015-02-13},
	date = {2015-02-15},
	langid = {english}
}

@article{urbanucci_overexpression_2012,
	title = {Overexpression of androgen receptor enhances the binding of the receptor to the chromatin in prostate cancer},
	volume = {31},
	issn = {1476-5594},
	doi = {10.1038/onc.2011.401},
	abstract = {Androgen receptor ({AR)} is overexpressed in the majority of castration-resistant prostate cancers ({CRPCs).} Our goal was to study the effect of {AR} overexpression on the chromatin binding of the receptor and to identify {AR} target genes that may be important in the emergence of {CRPC.} We have established two sublines of {LNCaP} prostate cancer ({PC)} cell line, one overexpressing {AR} 2-3-fold and the other 4-5-fold compared with the control cells. We used chromatin immunoprecipitation ({ChIP)} and deep-sequencing (seq) to identify {AR-binding} sites ({ARBSs).} We found that the number of {ARBSs} and the {AR-binding} strength were positively associated with the level of {AR} when cells were stimulated with low concentrations of androgens. In cells overexpressing {AR}, the chromatin binding of the receptor took place in 100-fold lower concentration of the ligand than in control cells. We confirmed the association of {AR} level and chromatin binding in two {PC} xenografts, one containing {AR} gene amplification with high {AR} expression, and the other with low expression. By combining the {ChIP-seq} and expression profiling, we identified {AR} target genes that are upregulated in {PC.} Of them, the expression of {ZWINT}, {SKP2} (S-phase kinase-associated protein 2 (p45)) and {FEN1} (flap structure-specific endonuclease 1) was demonstrated to be increased in {CRPC}, while the expression of {SNAI2} was decreased in both {PC} and {CRPC.} {FEN1} protein expression was also associated with poor prognosis in prostatectomy-treated patients. Finally, the knock-down of {FEN1} with small interfering {RNA} inhibited the growth of {LNCaP} cells. Our data demonstrate that the overexpression of {AR} sensitizes the receptor binding to chromatin, thus, explaining how {AR} signaling pathway is reactivated in {CRPC} cells.},
	pages = {2153-2163},
	number = {17},
	journaltitle = {Oncogene},
	shortjournal = {Oncogene},
	author = {Urbanucci, A and Sahu, B and Seppälä, J and Larjo, A and Latonen, L M and Waltering, K K and Tammela, T L J and Vessella, R L and Lähdesmäki, H and Jänne, O A and Visakorpi, T},
	date = {2012-04-26},
	note = {{PMID:} 21909140},
	keywords = {Animals, Binding Sites, Cell Line, Tumor, Chromatin, Flap Endonucleases, Gene Amplification, Gene Expression Profiling, Humans, Intracellular Signaling Peptides and Proteins, Male, Mice, Nuclear Proteins, Nucleic Acid Amplification Techniques, Prostatic Neoplasms, Receptors, Androgen, S-Phase Kinase-Associated Proteins, Transplantation, Heterologous}
}

@article{pemberton_genome-wide_2014,
	title = {Genome-wide co-localization of Polycomb orthologs and their effects on gene expression in human fibroblasts},
	volume = {15},
	issn = {1465-6914},
	doi = {10.1186/gb-2014-15-2-r23},
	abstract = {{BACKGROUND:} Polycomb group proteins form multicomponent complexes that are important for establishing lineage-specific patterns of gene expression. Mammalian cells encode multiple permutations of the prototypic Polycomb repressive complex 1 ({PRC1)} with little evidence for functional specialization. An aim of this study is to determine whether the multiple orthologs that are co-expressed in human fibroblasts act on different target genes and whether their genomic location changes during cellular senescence.
{RESULTS:} Deep sequencing of chromatin immunoprecipitated with antibodies against {CBX6}, {CBX7}, {CBX8}, {RING1} and {RING2} reveals that the orthologs co-localize at multiple sites. {PCR-based} validation at representative loci suggests that a further six {PRC1} proteins have similar binding patterns. Importantly, sequential chromatin immunoprecipitation with antibodies against different orthologs implies that multiple variants of {PRC1} associate with the same {DNA.} At many loci, the binding profiles have a distinctive architecture that is preserved in two different types of fibroblast. Conversely, there are several hundred loci at which {PRC1} binding is cell type-specific and, contrary to expectations, the presence of {PRC1} does not necessarily equate with transcriptional silencing. Interestingly, the {PRC1} binding profiles are preserved in senescent cells despite changes in gene expression.
{CONCLUSIONS:} The multiple permutations of {PRC1} in human fibroblasts congregate at common rather than specific sites in the genome and with overlapping but distinctive binding profiles in different fibroblasts. The data imply that the effects of {PRC1} complexes on gene expression are more subtle than simply repressing the loci at which they bind.},
	pages = {R23},
	number = {2},
	journaltitle = {Genome biology},
	shortjournal = {Genome Biol.},
	author = {Pemberton, Helen and Anderton, Emma and Patel, Harshil and Brookes, Sharon and Chandler, Hollie and Palermo, Richard and Stock, Julie and Rodriguez-Niedenführ, Marc and Racek, Tomas and de Breed, Lucas and Stewart, Aengus and Matthews, Nik and Peters, Gordon},
	date = {2014-02-03},
	note = {{PMID:} 24485159}
}

@article{yu_clusterprofiler_2012,
	title = {{clusterProfiler:} an R Package for Comparing Biological Themes Among Gene Clusters},
	volume = {16},
	issn = {1536-2310, 1557-8100},
	shorttitle = {{clusterProfiler}},
	url = {http://online.liebertpub.com/doi/abs/10.1089/omi.2011.0118},
	doi = {10.1089/omi.2011.0118},
	number = {5},
	urldate = {2012-05-05},
	journal = {{OMICS:} A Journal of Integrative Biology},
	author = {Yu, Guangchuang and Wang, Li-Gen and Han, Yanyan and He, Qing-Yu},
	month = may,
	year = {2012},
	pages = {284--287},
}

@article{ashburner_gene_2000,
	title = {Gene Ontology: tool for the unification of biology},
	volume = {25},
	issn = {1061-4036},
	url = {http://dx.doi.org/10.1038/75556},
	doi = {10.1038/75556},
	shorttitle = {Gene Ontology},
	issue = {1},
	pages = {25-29},
	journaltitle = {Nat Genet},
	shortjournal = {Nat Genet},
	author = {Ashburner, Michael and Ball, Catherine A. and Blake, Judith A. and Botstein, David and Butler, Heather and Cherry, J. Michael and Davis, Allan P. and Dolinski, Kara and Dwight, Selina S. and Eppig, Janan T. and Harris, Midori A. and Hill, David P. and Issel-Tarver, Laurie and Kasarskis, Andrew and Lewis, Suzanna and Matese, John C. and Richardson, Joel E. and Ringwald, Martin and Rubin, Gerald M. and Sherlock, Gavin},
	urldate = {2010-04-13},
	date = {2000-05},
}

@article{kanehisa_kegg_2004,
	title = {The {KEGG} resource for deciphering the genome},
	volume = {32},
	issn = {0305-1048, 1362-4962},
	url = {http://nar.oxfordjournals.org/content/32/suppl_1/D277},
	doi = {10.1093/nar/gkh063},
	language = {en},
	issue = {suppl 1},
	pages = {D277-D280},
	journaltitle = {Nucleic Acids Research},
	shortjournal = {Nucl. Acids Res.},
	author = {Kanehisa, Minoru and Goto, Susumu and Kawashima, Shuichi and Okuno, Yasushi and Hattori, Masahiro},
	urldate = {2013-10-15},
	date = {2004},
	note = {{PMID:} 14681412},
}

@article{schriml_disease_2011,
	title = {Disease Ontology: a backbone for disease semantic integration},
	volume = {40},
	issn = {0305-1048, 1362-4962},
	url = {http://nar.oxfordjournals.org/content/40/D1/D940.long},
	doi = {10.1093/nar/gkr972},
	shorttitle = {Disease Ontology},
	issue = {D1},
	pages = {D940-D946},
	journaltitle = {Nucleic Acids Research},
	author = {Schriml, L. M. and Arze, C. and Nadendla, S. and Chang, Y.-W. W. and Mazaitis, M. and Felix, V. and Feng, G. and Kibbe, W. A.},
	urldate = {2012-03-01},
	date = {2011-11-12},
}


@article{croft_reactome_2013,
	title = {The Reactome pathway knowledgebase},
	volume = {42},
	issn = {0305-1048, 1362-4962},
	url = {http://nar.oxfordjournals.org/content/42/D1/D472.long},
	doi = {10.1093/nar/gkt1102},
	issue = {D1},
	pages = {D472-D477},
	journaltitle = {Nucleic Acids Research},
	author = {Croft, D. and Mundo, A. F. and Haw, R. and Milacic, M. and Weiser, J. and Wu, G. and Caudy, M. and Garapati, P. and Gillespie, M. and Kamdar, M. R. and Jassal, B. and Jupe, S. and Matthews, L. and May, B. and Palatnik, S. and Rothfels, K. and Shamovsky, V. and Song, H. and Williams, M. and Birney, E. and Hermjakob, H. and Stein, L. and {D'Eustachio}, P.},
	urldate = {2014-02-18},
	date = {2013-11-15},
}